Hypotension and cardiac arrest are observed in patients anesthetized with the volatile anesthetics, halothane and enflurane. These anesthetics are in wide clinical use today. Clinical and laboratory investigations have established that cardiovascular depressant effects of halothane and enflurane are due to a direct depression of myocardial contractility. Preliminary physiologial and biochemical evidence suggests that the cardiac sarcoplasmic reticulum might be the site at which halothane and enflurane exert their negative inotropic effects. The sarcoplasmic reticulum is the intracellular organelle which regulates Ca ions availability for muscle contraction. A kinetic mechanism of the Ca ion uptake and coupled ATPase activity of the sarcoplasmic reticulum has been described. In an attempt to understand the possible mechanism of cardiac depression by anesthetics this study will examine the specific changes caused by halothane and enflurane in individual steps in the previously described reaction pathway. Steady state and presteady state kinetic measurements will permit the quantification of anesthetic inhibition or stimulation in this subcellular preparation. This data will help in formulating pharmacological interventions to avoid anesthetic-induced cardiac depression in the operating room.